Related Experiment Video

Updated: Dec 3, 2025

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depola
10:45

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depola

Published on: January 13, 2012

16.3K

Arsenic compounds activate the MAPK and caspase pathways to induce apoptosis in OEC‑M1 gingival epidermal carcinoma

Ning-Ping Foo1, Chi-Lin Ko1, Chiao-Yun Chu2

  • 1Department of Emergency Medicine, An Nan Hospital, China Medical University, Tainan 70965, Taiwan, R.O.C.

Oncology Reports
|October 30, 2020
PubMed

Insights

Sodium arsenite (NaAsO2) and dimethylarsenic acid (DMA) show potential as oral cancer treatments. These arsenic compounds induce apoptosis in oral squamous carcinoma cells, suggesting a novel therapeutic avenue.

Area of Science:

  • Toxicology
  • Oncology
  • Cell Biology

Background:

  • Arsenic is a known environmental toxicant with established therapeutic uses, including arsenic trioxide for cancer treatment.
  • Oral cancer incidence is rising in Taiwan, often linked to lifestyle factors like tobacco, alcohol, and betel quid chewing.
  • The specific effects of arsenic compounds on oral cancer cells remain largely unexplored.

Purpose of the Study:

  • To investigate the potential anticancer effects of sodium arsenite (NaAsO2) and dimethylarsenic acid (DMA) on oral squamous carcinoma cells (OEC-M1).
  • To determine if these arsenic compounds can induce apoptosis and affect cell cycle progression in oral cancer cells.

Main Methods:

  • OEC-M1 oral squamous carcinoma cells were treated with NaAsO2 and DMA.
  • Morphological changes indicative of apoptosis were observed.
  • Annexin V/PI double staining was performed to confirm apoptosis.
  • Cell survival rates and cell cycle distribution (subG1 and G2/M phases) were analyzed.
  • Western blotting was used to assess the activation of apoptotic markers (caspase-3, -8, -9, PARP) and MAPK pathways (JNK, ERK1/2, p38).

Main Results:

  • NaAsO2 and DMA induced morphological changes characteristic of apoptosis, such as cell rounding and membrane blebbing.
  • Annexin V/PI staining confirmed that both arsenic compounds significantly induced apoptosis in OEC-M1 cells.
  • Cell survival rates were significantly decreased, and the percentage of cells in subG1 and G2/M phases increased following treatment.
  • Cleavage of caspase-3, -8, -9, and PARP, along with phosphorylation of JNK, ERK1/2, and p38, was significantly activated.

Conclusions:

  • NaAsO2 and DMA effectively induce apoptosis in OEC-M1 oral squamous carcinoma cells.
  • These arsenic compounds activate both extrinsic and intrinsic apoptotic pathways via MAPK signaling.
  • The findings suggest that NaAsO2 and DMA hold promise as novel therapeutic agents for oral cancer.
Keywords:
sodium arsenitedimethylarsenic acidoral cancerOEC-M1apoptosiscaspase pathwayMAPK pathway

More Related Videos

In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration09:24

In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration

Published on: February 23, 2019

23.6K
Flow Cytometric Analysis of Apoptotic Biomarkers in Actinomycin D-Treated SiHa Cervical Cancer Cells13:53

Flow Cytometric Analysis of Apoptotic Biomarkers in Actinomycin D-Treated SiHa Cervical Cancer Cells

Published on: August 26, 2021

5.3K

Related Concept Videos

MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
7.4K
Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
13.2K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
7.7K
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
7.4K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
13.2K
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...
1.7K